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SHC016H

Sigma-Aldrich

MISSION® pLKO.1-puro Non-Target shRNA Control Transduction Particles, High Titer

Targets no known genes from any species

Synonym(s):

MISSION®, MISSION® Control Transduction Particles, negative control, negative shRNA control, non-target control, non-target shRNA, non-target shRNA control, shRNA control

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About This Item

UNSPSC Code:
41106609
NACRES:
NA.51

Quality Level

200

product line

MISSION®

concentration

≥1x109 VP/ml (via p24 assay)

shipped in

dry ice

storage temp.

−70°C

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General description

The MISSION pLKO.1-puro Non-Target shRNA Control Transduction Particles, High Titer contain an shRNA insert that does not target any known genes from any species, making it useful as a negative control in experiments using the MISSION shRNA library clones. This allows one to examine the effect of transduction of a short-hairpin on gene expression and interpret the knockdown effect seen with shRNA clones. Ampicillin and puromycin antibiotic resistance genes provide selection in bacterial or mammalian cells respectively. In addition, self-inactivating replication incompetent viral particles can be produced in packaging cells (HEK293T) by co-transfection with compatible packaging plasmids.
High titer virus is useful when performing in vivo research.
When conducting experiments using MISSION® shRNA clones, the proper controls should be a key element of your experimental design to allow for accurate interpretation of knockdown results. The MISSION Control Transduction Particles are a critical positive control to monitor transduction efficiency.
To see more application data, protocols, vector maps visit sigma.com/shrna.

Application

To see more application data, protocols, vector maps visit sigma.com/shrna.

Legal Information

MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

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Najim Lahrouchi et al.
Nature communications, 10(1), 1180-1180 (2019-03-14)
A failure in optic fissure fusion during development can lead to blinding malformations of the eye. Here, we report a syndrome characterized by facial dysmorphism, colobomatous microphthalmia, ptosis and syndactyly with or without nephropathy, associated with homozygous frameshift mutations in

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